Natural Killer Cells at Ease
Atherosclerosis Is Not Affected by Genetic Depletion or Hyperactivation of Natural Killer Cells
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Atherosclerosis is a lipid-driven, chronic inflammatory disorder that is characterized by the formation of leukocyte-rich plaques in large- and medium-sized arteries. Plaque macrophages form lipid-laden foam cells and eventually fail to clear the overwhelming number of apoptotic cells (failure of efferocytosis), forming a necrotic core. Other immune cells like T- and B-cell subsets contribute to atheroprogression by controlling the inflammatory milieu. The subject of the present work1 concerns the role of natural killer (NK) cells in atherosclerosis progression.
Article, see p 47
NK cells are found at an average of 1 to 2 cells per lesion section.1 NK cells are potent immune cells protecting the host from viral infections and tumor formation. If a host cell lacks surface MHC-I (major histocompatibility complex I), being in a state of missing self, NK cells will kill this cell. NK cells also display immune-regulatory features and are capable of influencing antigen-specific T-cell responses. In the course of cardiovascular disease, the number of NK cells decreases in patients with stable angina or non–ST-segment–elevation myocardial infarction without affecting their cytokine expression profile.2 Until now,1 the role of NK cells in atherosclerosis had remained unclear and controversial.
In this issue of Circulation Research, Nour-Eldine et al1 show that NK cells are not involved in atherosclerosis.
A first study investigating NK cell activity in atherosclerosis assessed beige mice. Beige mice carry a mutation of the Lyst gene impairing NK …